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1 Baylor College of Medicine, Cardiology Research, Veterans Affairs Medical Center, Houston, Texas 77030; 2 Department of Exercise and Sport Sciences and Physiology and the Center for Exercise Science, University of Florida, Gainesville, 32611; 3 Geriatric Research, Education and Clinical Center, Department of Veterans Affairs Medical Center, and 4 Division of Cardiology, University of Florida College of Medicine, Gainesville, Florida 32610; 5 Department of Exercise and Health Science, Yamaguchi University, Yamaguchi, Japan 753; and 6 Department of Clinical Pathology, Gyeongsang National University School of Medicine, Chinju, Korea 660-702
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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We examined
the effects of 3 days of exercise in a cold environment on the
expression of left ventricular (LV) heat shock proteins (HSPs) and
contractile performance during in vivo ischemia-reperfusion (I/R). Sprague-Dawley rats were divided into the following three groups
(n = 12/group): 1) control, 2)
exercise (60 min/day) at 4°C (E-Cold), and 3) exercise (60 min/day) at 25°C (E-Warm). Left anterior descending coronary
occlusion was maintained for 20 min, followed by 30 min of reperfusion.
Compared with the control group, both the E-Cold and E-Warm groups
maintained higher (P < 0.05) LV developed pressure,
first derivative of pressure development over time (+dP/dt),
and pressure relaxation over time (
dP/dt) throughout I/R.
Relative levels of HSP90, HSP72, and HSP40 were higher
(P < 0.05) in E-Warm animals compared with both
control and E-Cold. HSP10, HSP60, and HSP73 did not differ between
groups. Exercise increased manganese superoxide dismutase (MnSOD)
activity in both E-Warm and E-Cold hearts (P < 0.05).
Protection against I/R-induced lipid peroxidation in the LV paralleled
the increase in MnSOD activity whereas lower levels of lipid
peroxidation were observed in both E-Warm and E-Cold groups compared
with control. We conclude that exercise-induced myocardial protection
against a moderate duration I/R insult is not dependent on increases in myocardial HSPs. We postulate that exercise-associated cardioprotection may depend, in part, on increases in myocardial antioxidant defenses.
endurance exercise; heart; radicals; lipid peroxidation; antioxidant enzymes
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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IT IS CLEAR THAT ENDURANCE exercise training provides myocardial protection against ischemia-reperfusion (I/R) injury (2, 4, 5, 9, 15, 19, 25, 27). Indeed, both short-term (i.e., days) and long-term (i.e., months) exercise training enhances myocardial recovery after an I/R insult as evidenced by an improved recovery of cardiac contractile performance and reduced oxidative damage to the myocardium (9, 25). The exact biochemical mechanisms responsible for this protection continue to be debated. Nonetheless, it has been argued that elevated myocardial levels of heat shock protein (HSP) 72, and perhaps other HSPs (e.g., HSP10, HSP40, HSP60, and HSP90), play a significant role in the exercise-induced improvement in myocardial protection during I/R (for reviews, see Refs. 20 and 21).
Although an exercise-induced increase in myocardial HSP72 is a potential mechanism to explain the cardioprotection associated with exercise, recent work by Taylor et al. (27) indicates that exercise training in a cold environment does not elevate myocardial levels of HSP72 but improves myocardial performance postischemia in an isolated working heart model. Taylor et al. concluded that whereas increases in myocardial HSP72 can contribute to improved postischemic function, other mechanisms must be responsible for the exercise-induced cardioprotection in their experiments.
With the use of an in vivo model of I/R, the current experiments expand on the work of Taylor et al. (27) by exploring other potential mechanisms that could contribute to the exercise-induced myocardial protection during an I/R insult. In particular, we hypothesized that whereas exercise in a cold environment does not upregulate the expression of myocardial HSP72, this type of exercise could increase other important stress proteins in the heart and/or enhance myocardial antioxidant defenses. To test this hypothesis, animals were exercise trained in both warm and cold environments. Myocardial responses to in vivo I/R were then examined and myocardial levels of stress proteins and the activities of primary antioxidant enzymes were assessed.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Animals and Experimental Design
This experimental protocol was approved by the University of Florida Animal Care and Use Committee and followed the guidelines established by the American Physiological Society for the use of animals in research. Female Sprague-Dawley rats (4 mo old) were randomly assigned to one of three experimental groups (n = 12/group): 1) control, 2) 3-5 consecutive days of treadmill exercise in a cold (4°C) environment (E-Cold), and 3) 3-5 consecutive days of treadmill exercise in a warm (25°C) environment (E-Warm). Each of these three groups was further divided into two surgical groups: sham surgery and I/R surgery. During the experimental period, all groups were maintained on a 12:12-h light-dark cycle and provided rat chow and water ad libitum.Exercise Training Protocol
The animals selected to engage in exercise training were habituated to treadmill exercise by daily treadmill running for 3-5 consecutive days. Ambient temperature in which training occurred was either 25°C or 4°C. The first day of exercise began with a 5-min exercise bout; this duration was increased by 10-15 min per day during the next 4 days. Control animals were placed in a nonmoving treadmill. After this habituation to exercise training, the exercise-trained animals were then exercised for 3-5 consecutive days of treadmill exercise, 60 min/day, 30 m/min, 0% grade, at ~70% maximal O2 consumption (18). Mild electrical shocks were used sparingly to motivate animals to run. Colonic temperature was measured before and after each 60-min exercise bout. The decision to exercise train animals for 3-5 days at this work rate was based on previous work from our laboratory (unpublished observations), indicating that this training protocol promotes myocardial expression of HSP72 and provides cardioprotection during an in vivo I/R insult.In Vivo Protocol for Studying Myocardial Responses During I/R
In vivo I/R was performed 24 h after the last exercise training session. Animals were anesthetized with 30 mg/kg of pentobarbital sodium and ventilated with room air with the use of a small animal ventilator (Kent Scientific; Litchfield, CT). Throughout the surgery, body temperature was monitored via a rectal thermistor probe. Body temperature was maintained at ~37 ± 1°C with the use of a heated operating platform and appropriate heating lamps. Cardiac rhythm was monitored continuously via a standard electrocardiogram (lead II).The chest was opened by a left thoracotomy and a ligature was placed around the left anterior descending coronary artery (LCA) close to its origin (ligature ends were exteriorized). At this point, any animals exhibiting significant ventricular arrhythmias were eliminated from the study. Coronary occlusion was achieved by passing both ends of the ligature through a small plastic tube, which was then pressed against the surface of the heart directly above the LCA. The resulting arterial occlusion was maintained for 20 min by clamping the plastic tube and ligature with a small hemostat. This duration of ischemia results in myocardial stunning without significant infarction (3). Reperfusion duration was 30 min and was achieved by removing the clamp and the tube. When necessary, gentle massage of the nonischemic portion of the heart was used to convert ventricular fibrillation into a normal sinus rhythm. Animals exhibiting >3 episodes of ventricular fibrillation were eliminated from the study. Sham surgery included all surgical interventions with the exception of coronary occlusion.
Validation of Coronary Occlusion and Reperfusion
The aforementioned technique of coronary occlusion has been shown to be effective by other investigators (2, 15). More importantly, we have validated that complete coronary occlusion, consistently resulting in ischemia in ~60% of the myocardium, is achieved in our hands (author's unpublished observations). Furthermore, we (25) have also performed experiments to ensure that reperfusion is adequately achieved in this model.Measurement of Left Ventricular Developed Pressure and dP/dt
To monitor cardiovascular function during the I/R protocol, an arterial cannula was introduced via the carotid artery into the left ventricle. Left ventricular developed pressure (LVDP), first derivative of pressure development over time (+dP/dt), and first derivative of pressure relaxation over time (dP/dt) were measured by using a pressure transducer interfaced with a computerized heart performance analysis system (Digi-Med; Louisville, KY).
Tissue Preparation
Selected biochemical properties of the ventricular myocardium were studied in all experimental groups. To determine the antioxidant capacity in the hearts of all experimental groups, small samples of the LV were removed, rinsed free of blood in ice-cold antioxidant buffer (100 µM EDTA, 50 mM NaHPO4, and 1 mM BHT; pH 7.4), and quickly frozen in liquid nitrogen. These samples were later assayed to determine the concentration of protein thiols as well as the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT).Furthermore, LV tissue that was inferior to the LCA occlusion site was quickly removed, divided into three sections, and frozen in liquid nitrogen for subsequent biochemical analysis of lipid peroxidation and measurement of the relative levels of HSP10, HSP40, HSP60, HSP72, HSP73, and HSP90.
Biochemical Assays
To assess the effects of both exercise training and I/R on the myocardium, we measured tissue lipid peroxidation, protein thiols, and the activities of antioxidant enzymes. Sections of the LV myocardium were minced and homogenized in 100 mM cold phosphate buffer with 0.05% bovine serum albumin (1:20 wt/vol; pH 7.4). Homogenization was achieved by using 40 passes of the homogenate in a tight-fitting Potter-Elvehjem homogenizer. Homogenates were then centrifuged (3°C) for 10 min at 400 g. The supernatant was decanted and assayed to determine total protein content along with the activities of SOD (EC1.15.1.1), CAT (EC1.11.1.6), and GPx (EC1.11.1.9). Protein content was determined using methods described by Bradford (6). In sham surgery groups, the supernatant was then assayed to determine the activities of both manganese SOD (MnSOD) and copper-zinc SOD (Cu/ZnSOD) using the cytochrome c reduction technique of McCord and Fridovich (23). GPx and CAT activity were determined in the LV as described by Flohe and Gunzler (11) and Aebi (1), respectively. In our laboratory, the coefficients of variation for SOD, GPx, and CAT were ~2, 3, and 5%, respectively. These and all other biochemical assays were performed in triplicate at 25°C and samples from all experimental groups were assayed on the same day to avoid interassay variation.Protein Thiol Measurements
Protein oxidation was assessed by spectrophotometric measurement of LV protein thiols, as described by Jocelyn (16). This assay measures the quantity and proportion of sulfhydryl (SH) groups within tissue. Briefly, total cellular thiols were determined by mixing 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB; a SH reagent) with tissue homogenate and quantifying spectrophotometrically at 412 nm. DTNB was then reacted with homogenate after acid precipitation of proteins. Protein-bound thiol content was obtained mathematically by subtracting the nonprotein-bound thiol concentration from the total thiol concentration.Lipid Peroxidation Measurements
To determine the amount of oxidative damage in the heart, LV levels of two by-products of lipid peroxidation were measured. Lipid hydroperoxides were quantified using the ferrous oxidation-xylenol orange technique reported by Hermes-Lima et al. (13). Briefly, after the tissue was homogenized in methanol, the membrane peroxides were mixed in solution with an iron source (FeSO4), an acid (H2SO4), and a reactive dye (xylenol orange). In this mixture, the membrane peroxides oxidize Fe2+ to Fe3+ and the peroxides are reduced. The ionized acid assists in the reduction. The Fe3+ then reacts with the xylenol orange to form a Fe3+-xylenol orange complex. Originally yellow in dye form, the Fe3+-xylenol complex changes to a purplish color that can be detected spectrophotometrically at 580 nm. Cumene hydroperoxide was used to generate a standard curve for this assay.In addition to lipid hydroperoxides, total 8-isoprostane was quantified by competitive enzyme immunoassay (EIA) as per the manufacturer's instruction (Cayman Chemical; Ann Arbor, MI). Measurement of 8-isoprostane, a member of the eicosanoid family, is based on the competition between 8-isoprostane and an 8-isoprostane-acetylcholinesterase conjugate for a limited amount of 8-isoprostane polyclonal antiserum. Briefly, after homogenization in methanol, samples are extracted and hydrolyzed via incubations in 100% ethanol and 15% potassium hydroxide. Resultant samples are then purified on a methanol-activated Sep-Pak C18 column and evaporated to dryness using a Supelco vacuum centrifugation system. The remaining residue is then redissolved in EIA buffer, placed in microplates coated with antibody, and mixed with antiserum to 8-isoprostane and 8-isoprostane linked to acetylcholinesterase. After a 24-h incubation, wells are washed free of unbound reagents, and Ellman's reagent is added to facilitate spectrophotometric measurement at 412 nm. Standard curves constructed using known concentrations of 8-isoprostane are used to quantify total 8-isoprostane concentration in the samples.
Immunoblotting
To determine the effects of training on induction of myocardial HSPs, we performed polyacrylamide gel electrophoresis and immunoblotting using a modification of techniques described by Locke et al. (21). Briefly, LV samples from I/R animals were homogenized and one-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis was performed to separate proteins by molecular weight. The percentage of polyacrylamide used in gels varied as a function of the molecular weight of the individual HSP as follows: HSP90 (10%), HSP73 (12.5%), HSP72 (12.5%), HSP60 (12.5%), HSP40 (12.5%), and HSP10 (15%). After separation, proteins were transferred to nitrocellulose membranes (0.45 mm thick, Bio-Rad; Hercules, CA) using the Bio-Rad transblot electrophoretic transfer cell at a constant voltage of 100 V for 1 h. After protein transfer, the nitrocellulose membranes were blocked for 2 h using either 1% bovine serum albumin or 5% nonfat dry milk. Blots were incubated for 2 h with the following antibodies: rabbit polyclonal anti-HSP40, mouse monoclonal anti-HSP72, rabbit polyclonal anti-CPN10, mouse monoclonal anti-HSP60, rat monoclonal anti-HSP90, or rat monoclonal anti-HSP70 (Stress Gen; Victoria, Canada). Antibodies were then reacted with the appropriate secondary antibody conjugated to alkaline phosphatase before incubation with bromochloroindolyl phosphate-nitro blue tetrazolium substrate (Sigma; St. Louis, MO). Quantification of the bands from the immunoblots was performed using computerized densitometry and NIH Image Analysis software. Standard curves were constructed during preliminary experiments to assure linearity.Data Analysis
Significance was established a priori at P < 0.05. All dependent variables were analyzed using analysis of variance software (Systat, SPSS). Where appropriate, Tukey's honestly significant difference test was applied post hoc.| |
RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Colonic Temperature During Exercise
Sixty minutes of exercise in the cold (4°C) environment did not result in a significant increase (P > 0.05) in colonic temperature (preexercise 38.2 ± 0.1°C; postexercise 38.1 ± 0.2°C). Hence, it seems unlikely that myocardial temperature increased significantly in these conditions. In contrast, 60 min of exercise in the thermoneutral (25°C) environment resulted in a significant rise (P < 0.05) in colonic temperature from 37.6 ± 0.2°C (preexercise) to 41.1 ± 0.2°C (postexercise).Myocardial Performance During I/R
Successful I/R protocols were performed on 12 animals from each experimental group. Ventricular fibrillation mandated exclusion of five control animals, two E-Warm animals, and two E-Cold animals. Figure 1 contains the mean values for LVDP during preischemia, ischemia, and after reperfusion in animals from all experimental groups. No differences existed (P > 0.05) between groups in these measures before ischemia. However, compared with control, both E-Cold and E-Warm animals maintained higher (P < 0.05) LVDP throughout both ischemia and reperfusion. Identical results were found for LV +dP/dt anddP/dt during I/R
(data not shown).
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Biochemical Measurements
Myocardial HSP content.
To determine if the relative levels of HSP10, 40, 60, 72, 73, and 90 were elevated in the hearts from exercise-trained animals, portions of
the LV from control, E-Cold, and E-Warm animals were analyzed for the
relative levels of HSP isoforms by using Western blotting. The results
revealed that myocardial levels of HSP40, HSP72, and HSP90 were
significantly greater (P < 0.05) in the LV of E-Warm
animals compared with both control and E-Cold animals (Fig.
2, A-C).
Whereas a trend toward increased HSP90 content was apparent in E-Cold
compared with control, this difference did not reach statistical
significance (P = 0.85). Exercise training (both
environmental conditions) did not alter (P > 0.05)
ventricular levels of HSP10, HSP60, and HSP73 (Fig.
3, A-C).
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Myocardial antioxidant enzyme activity.
To determine if exercise training altered myocardial antioxidant
capacity we measured the activities of MnSOD, Cu/ZnSOD, CAT, and GPx in
the LV of animals from all experimental groups. These data are
presented in Table 1. The results
revealed that compared with control, exercise training elevated
(P < 0.05) myocardial activity of MnSOD in both E-Cold
and E-Warm animals. In contrast, exercise training (E-Cold and E-Warm
animals) did not alter the activities of Cu/ZnSOD or CAT in the LV.
Also, myocardial GPx activity was greater (P < 0.05)
in E-Cold animals compared with both control and E-Warm animals.
Antioxidant enzyme activities were assayed in LV tissues from sham
surgery animals and, therefore, do not reflect the impact of
ischemia or reperfusion on enzyme activities.
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Myocardial lipid peroxidation and protein thiols.
To determine if the exercise-induced improvement in myocardial
contractile performance after an I/R insult was associated with
improved protection against oxidative stress, we measured two markers
of lipid peroxidation. Our results indicated that in hearts exposed to
I/R, myocardial levels of both lipid hydroperoxides, and 8-isoprostane
were lower (P < 0.05) in both E-Cold and E-Warm animals compared with control animals (Fig.
4). More importantly, it should be noted
that 8-isoprostane concentrations were also lower in both E-Warm sham
and E-Cold sham groups compared with control sham (P < 0.05). These results indicate that exercise training in both warm and
cold environments provided myocardial protection against I/R-induced
lipid peroxidation. This was the result of a lower sham or
"unstressed" level of lipid peroxidation.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Overview of Principal Findings
Our data indicate that exercise training in both a cold and warm environment provides myocardial protection as indicated by improved cardiac contractile performance during an in vivo I/R protocol designed to result in myocardial stunning. Exercise in the warm environment was associated with significant increases in the relative levels of myocardial HSP40, HSP72, and HSP90. However, exercise in the cold environment did not alter myocardial HSP levels. Hence, we interpret these results as evidence that the exercise training-induced protection against in vivo I/R injury can be achieved without an increase in myocardial HSPs. Because exercise training (both cold and warm environments) was associated with elevated myocardial antioxidant defenses and a decrease in I/R-induced myocardial lipid peroxidation, we postulate exercise-induced cardioprotection is due, in part, to an elevation in cardiac antioxidant defenses.Exercise Training Improves Myocardial Performance During I/R Without Elevation in HSPs
Our data indicate that short-term (3-5 days) endurance exercise training results in myocardial protection against I/R injury, as evidenced by the improved cardiac pressure generation during both ischemia and reperfusion (Fig. 1). These results agree with previous reports by others (21, 27).Our results also indicate that exercise-induced cardioprotection against I/R-induced injury does not require an elevation in myocardial levels of HSPs. Nonetheless, there is convincing evidence that HSP72 as well as other HSPs can contribute to myocardial protection against I/R injury. Indeed, recent studies (7, 22, 24) involving transfection of constructs into cultured cells and transgenic animal models have provided direct evidence that HSP72 is a cytoprotective protein. For example, studies (7, 22, 24) employing transgenic mice overexpressing HSP72 transgene products in their myocardium have provided strong evidence for HSP72-mediated myocardial protection during an I/R insult. Therefore, in the current experiments, the increases in myocardial levels of HSPs (i.e., HSP40, HSP72, and HSP90) after exercise bouts at room temperature are a potential contributor to the improved myocardial protection against I/R injury. However, our results reveal that the exercise training in a cold environment can provide protection against I/R-induced myocardial injury in vivo without increasing HSPs in the heart (i.e., HSP10, HSP40, HSP60, HSP72, HSP73, and HSP90). These data support and extend the findings of Taylor et al. (27), who reported that HSP72 is not the factor directly responsible for the exercise-induced myocardial protection after an in vitro I/R insult. Recently, however, Harris and Starnes (12) reported that preventing a rise in core temperature during chronic exercise, thus preventing accumulation of myocardial HSP72, abolishes the cardioprotection observed when core temperature rises during training resulting in increased myocardial HSP72. Collectively, we interpret these results as evidence that exercise training promotes complex biochemical alterations, other than an increased expression of major HSPs, capable of providing myocardial protection against an I/R insult involving ischemia of short-to-moderate duration.
Whereas several mechanisms could contribute to the training-induced cardioprotection, an exercise-induced upregulation in cardiac antioxidant capacity is a potential contributor. In this regard, it is well known that reactive oxygen species (ROS) are produced during I/R and are important contributors to I/R-induced myocardial injury (for a review, see Ref. 10). Furthermore, administration of ROS scavengers has been shown to attenuate I/R-induced cardiac injury (3). In the current experiments, exercise training promoted an upregulation of MnSOD activity in hearts from both E-Cold- and E-Warm-trained animals. Hence, we postulate that the training-induced increase in myocardial antioxidant capacity is a contributor to the cardioprotection associated with exercise. Yamashita et al. (28) reached similar conclusions. Interestingly, in a recent study by Harris and Starnes (12), transient changes in the activities of Cu/ZnSOD and MnSOD, as well as CAT, were reported after exercise training of various durations with or without changes in core temperature. Changes in enzyme activities were noted only with exercise training lasting 3 wk, and, because antioxidant activities returned to sedentary levels by 9 wk of training, changes in antioxidant defenses were ruled out as a contributing factor in the exercise-associated cardioprotection. Nonetheless, it remains unclear whether an increase in myocardial antioxidant capacity is the primary mechanism responsible for the cardioprotection associated with short-term exercise or whether an augmented antioxidant capacity is simply one of many redundant protective mechanisms affected by exercise training.
Influence of Body Temperature on Exercise-Induced HSP Expression
The component of exercise that is responsible for increasing the expression of myocardial HSPs continues to be investigated. A variety of stresses associated with exercise could contribute to the elevation in myocardial levels of HSPs. For example, heat stress, hypoxia, production of ROS, and stretching of cardiac myocytes are all potential contributors to HSP synthesis (see Ref. 17 for a review). In our experiments, when the exercise-induced rise in body temperature was prevented by exercise in the cold, myocardial levels of HSPs in E-Cold animals were not elevated above control. This finding indicates that the rise in body temperature during exercise is an essential component of the exercise-induced expression of myocardial HSP72 as well as other HSPs. Others have reached a similar conclusion (12, 27).Finally, whereas our results and those of others (12, 27) indicate that an exercise-induced increase in body temperature is required for an exercise-induced elevation in myocardial levels of HSPs, these findings differ from the work of others (26). Skidmore et al. (26) reported that when colonic temperature was maintained at resting temperature during exercise (i.e., exercise in a cool environment), small but significant exercise-induced increases in myocardial levels of HSP72 occurred. Close examination of these studies does not provide an explanation for the divergent findings; additional research is required to resolve this controversy.
In conclusion, to our knowledge, this is the first experiment to examine the effects of exercise training in a cold environment on cardioprotection during in vivo I/R. Furthermore, we also examined metabolic factors that might contribute to this exercise-induced protection during I/R (i.e., myocardial HSPs and antioxidant enzymes). The major finding of this study was that exercise-induced myocardial protection against an I/R insult is not dependent on increases in the levels of myocardial HSP10, HSP40, HSP60, HSP72, HSP73, or HSP90. Whereas numerous mechanisms could contribute to the training-induced cardioprotection, it seems likely that an exercise-induced upregulation in cardiac antioxidant capacity is a contributor. It is unclear if the exercise-induced increase in myocardial antioxidant capacity is the primary mechanism to explain the myocardial protection associated with exercise or if the improved antioxidant capacity is simply one of several protective mechanisms influenced by exercise training. Determining the mechanisms responsible for the exercise-induced cardioprotection is an important area for future research.
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ACKNOWLEDGEMENTS |
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This work was supported by a grant-in-aid from the American Heart Association, Florida Affiliate (to S. K. Powers) and by a contract with the Department of Defense (to J. L. Mehta).
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FOOTNOTES |
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Address for reprint requests and other correspondence: S. K. Powers, Dept. of Exercise and Sport Sciences and Physiology, Center for Exercise Science, Univ. of Florida, Gainesville, FL 32611 (E-mail: spowers{at}hhp.ufl.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 14 August 2000; accepted in final form 18 June 2001.
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TOP
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METHODS
RESULTS
DISCUSSION
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